Novel concepts on the role of prostaglandins on luteal maintenance and maternal recognition and establishment of pregnancy in ruminants
Novel concepts on the role of prostaglandins on luteal maintenance and maternal recognition and establishment of pregnancy in ruminants
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DOI：
10.3168/jds.2015-10335
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发表时间：
2016-07-01
影响因子：
3.5
通讯作者：
McCracken, John A.
中科院分区：
文献类型：
--
作者：
Arosh, Joe A.;Banu, Sakhila K.;McCracken, John A.
在反刍动物中，妊娠早期的黄体(CL)对黄体溶解具有抵抗力。前列腺素(PG)E-2被认为是一种黄体保护介质。早期的研究表明，在反刍动物的母体识别妊娠过程中，来自胚胎或妊娠子宫的一个因子(S)通过子宫-卵巢丛(UOP)局部准备卵巢，并保护CL免受黄体溶解。胚胎抗黄体溶解或黄体保护作用的局部性质排除了蛋白质在反刍动物妊娠子宫和CL之间运输或作用的任何直接作用。在MRP过程中，妊娠滋养细胞分泌的干扰素tau(IFNT)抑制子宫内膜PGF(2α)的搏动性释放，增加子宫内膜PGE(2)。我们最近的研究表明：(1)在绵羊ESP过程中，黄体PG的生物合成选择性地指向PGF(2α)和PGE(2)；(2)妊娠早期CL抵抗黄体溶解的能力可能是由于增加了PGE(2)的生物合成和信号转导；(3)在绵羊ESP过程中，子宫内膜PGE_1通过FOP血管通路从子宫输送到CL。宫内联合应用IFNT和前列腺素E-2合成酶-1(PGES-1)抑制剂可重建子宫内膜PGF(2α)，使CL起搏和消退。相反，宫内联合应用IFNT和PGES-1抑制剂以及卵巢内应用前列腺素E可以挽救CL。总之，这些积累的信息提供了令人信服的证据，表明CL在妊娠诱导的子宫内膜PGE(2)诱导下产生的PGE(2)可能抵消PGF(2α)的黄体溶解效应，作为反刍动物MRP或ESP过程中的一种额外的黄体保护机制。靶向PGE(2)的生物合成和选择性地在子宫内膜或CL中传递信号可能会提供黄体保护治疗，以提高反刍动物的繁殖效率。
In ruminants, the corpus luteum (CL) of early pregnancy is resistant to luteolysis. Prostaglandin (PG)E-2 is considered a luteoprotective mediator. Early studies indicate that during maternal recognition of pregnancy (MRP) in ruminants, a factor(s) from the conceptus or gravid uterus readies the ovary locally through the utero-ovarian plexus (UOP) and protects the CL from luteolysis. The local nature of the embryonic antiluteolytic or luteoprotective effect precludes any direct effect of a protein transported or acting between the gravid uterus and CL in ruminants. During MRP, interferon tau (IFNT) secreted by the trophoblast of the conceptus inhibits endometrial pulsatile release of PGF(2 alpha) and increases endometrial PGE(2). Our recent studies indicate that (1) luteal PG biosynthesis is selectively directed toward PGF(2 alpha), at the time of luteolysis and toward PGE(2) at the time of establishment of pregnancy (ESP); (2) the ability of the CL of early pregnancy to resist luteolysis is likely due to increased intraluteal biosynthesis and signaling of PGE(2); arid (3) endometrial PGE, is transported from the uterus to the CL through the FOP vascular route during ESP in sheep. Intrauterine co-administration of IFNT and prostaglandin E-2 synthase 1 (PGES-1) inhibitor reestablishes endometrial PGF(2 alpha), pulses and regresses the CL. In contrast, intrauterine co-administration of IFNT and PGES-1 inhibitor along with intraovarian administration of PGE, rescues the CL. Together, the accumulating information provides compelling evidence that PGE(2) produced by the CL in response to endometrial PGE(2) induced by pregnancy may counteract the luteolytic effect of PGF(2 alpha), as an additional luteoprotective mechanism during MRP or ESP in ruminants. Targeting PGE(2) biosynthesis and signaling selectively in the endometrium or CL may provide luteoprotective therapy to improve reproductive efficiency in ruminants.